Pulmonary heart disease (cor pulmonale) is the state showing right ventricular pressure load or dysfunction of right ventricle by increase in pulmonary vascular resistance caused by diseases of lung parenchyma, pulmonary vascular diseases or extrapulmonary diseases which cause alveolar hypoventilation. Based on clinical progress and pathologic state, pulmonary heart disease is classified into three groups, that is, acute pulmonary heart, subacute pulmonary heart and chronic pulmonary heart, and the type of primary diseases of the three groups are different from each other. The representative cause of acute pulmonary heart is pulmonary thromboembolism in which right ventricle is prominently dilated without the time of presenting right ventricular hypertrophy, followed by right heart failure. The causes of subacute pulmonary heart disease include multiple or recurrent lung embolism, but its pathologic state is similar to that of acute pulmonary heart disease. The causes of chronic pulmonary heart disease include chronic occlusive pulmonary disease and pulmonary hypertension. Chronic pulmonary heart disease accompanies hyperplasia of right ventricular heart muscle, respiratory difficulty when moving, cardiopalmus and edema, and its prognosis is bad. Fibrinoid formation or thrombus formation in the lung plays a pivotal role in development of these pathological stage.
Current therapeutic methods for treating pulmonary heart disease are based on therapy and control of the primary diseases. There is no effective etiotropic methods and only nosotropic treatment is performed.
As for the model animals used for clarifying the pathologic state and for studying effective therapeutic method or the like, monocrotaline-treated rat models were employed as the model animal for pulmonary hypertension. This model is pathologically characterized mainly by hyperplasia of tunica media of muscular pulmonary artery, muscularization of pulmonary arteriole and hyperplasia of intraalveolar septa.
However, in the conventional monocrotaline-rat model animal, fibrinoid formation and thrombus formation in the lung are scarcely observed in the development of the diseased state, and the monocrotaline-rat model animal is positioned as a model of the so called secondary pulmonary hypertension in which pulmonary hypertension and interstitial pneumonia are complicated. Thus, the monocrotaline-rat model is insufficient for clarifying the pathologic state of testing pulmonary heart and for studying a therapeutic method of testing pulmonary heart depending on the severity of the disease. There is no promising therapeutic method for pulmonary heart.